Overview
<table class="infobox infobox-cell">
<tr>
<th class="infobox-header" colspan="2">Median Eminence</th>
</tr>
<tr>
<td class="label">Taxonomy</td>
<td>ID</td>
</tr>
<tr>
<td class="label">Allen Brain Cell Atlas</td>
<td>[Search](https://portal.brain-map.org/atlases-and-data/bkp/abc-atlas)</td>
</tr>
<tr>
<td class="label">Cell Ontology (CL)</td>
<td>[Search](https://www.ebi.ac.uk/ols4/ontologies/cl/)</td>
</tr>
<tr>
<td class="label">Human Cell Atlas</td>
<td>[Search](https://www.humancellatlas.org/)</td>
</tr>
<tr>
<td class="label">CellxGene Census</td>
<td>[Search](https://cellxgene.cziscience.com/)</td>
</tr>
</table>
The median eminence (ME) is a circumventricular organ located in the floor of the third ventricle at the base of the hypothalamus. This neuroendocrine structure lacks a complete blood-brain barrier, allowing direct communication between the brain and peripheral circulation. The ME serves as the primary gateway for hypothalamic releasing and inhibiting hormones to reach the anterior pituitary gland via the hypophyseal portal system[@rodriguez2022]. It contains tanycytes, axonal terminals from hypothalamic neurons, and portal capillaries that regulate neuroendocrine function[@prevot2021].
Multi-Taxonomy Classification
Taxonomy Database Cross-References
External Database Links
...Overview
<table class="infobox infobox-cell">
<tr>
<th class="infobox-header" colspan="2">Median Eminence</th>
</tr>
<tr>
<td class="label">Taxonomy</td>
<td>ID</td>
</tr>
<tr>
<td class="label">Allen Brain Cell Atlas</td>
<td>[Search](https://portal.brain-map.org/atlases-and-data/bkp/abc-atlas)</td>
</tr>
<tr>
<td class="label">Cell Ontology (CL)</td>
<td>[Search](https://www.ebi.ac.uk/ols4/ontologies/cl/)</td>
</tr>
<tr>
<td class="label">Human Cell Atlas</td>
<td>[Search](https://www.humancellatlas.org/)</td>
</tr>
<tr>
<td class="label">CellxGene Census</td>
<td>[Search](https://cellxgene.cziscience.com/)</td>
</tr>
</table>
The median eminence (ME) is a circumventricular organ located in the floor of the third ventricle at the base of the hypothalamus. This neuroendocrine structure lacks a complete blood-brain barrier, allowing direct communication between the brain and peripheral circulation. The ME serves as the primary gateway for hypothalamic releasing and inhibiting hormones to reach the anterior pituitary gland via the hypophyseal portal system[@rodriguez2022]. It contains tanycytes, axonal terminals from hypothalamic neurons, and portal capillaries that regulate neuroendocrine function[@prevot2021].
Multi-Taxonomy Classification
Taxonomy Database Cross-References
External Database Links
- [Allen Brain Cell Atlas](https://portal.brain-map.org/atlases-and-data/bkp/abc-atlas)
- [Cell Ontology](https://www.ebi.ac.uk/ols4/ontologies/cl/)
- [Human Cell Atlas](https://www.humancellatlas.org/)
- [CellxGene Census](https://cellxgene.cziscience.com/)
- [PanglaoDB](https://panglaodb.se/)
Anatomy and Structure
The ME is situated in the infundibular region of the hypothalamus, forming the median eminence of the tuber cinereum. Key cellular components include:
- Tanycytes: Specialized ependymal cells with long processes that extend into the ME, forming a barrier between the cerebrospinal fluid and portal blood. Tanycytes express thyroid hormone transporters (OATP1C1, MCT8) and regulate hormone passage into the brain[@bolborea2022].
- Neuronal terminals: Axon terminals from hypothalamic neurons (paraventricular nucleus, arcuate nucleus) release neurohormones into the perivascular space of the portal capillaries[@fowkes2021].
- Portal capillaries: A specialized capillary network that carries hypothalamic hormones directly to the anterior pituitary, bypassing the systemic circulation[@smith2022].
The ME receives input from multiple brain regions, including the preoptic area, arcuate nucleus, and paraventricular nucleus. These inputs regulate the secretion of releasing hormones including GnRH, CRH, TRH, GHRH, and somatostatin[@sapolsky2021].
Role in Neurodegenerative Diseases
Alzheimer's Disease
The ME shows pathological changes in AD, including accumulation of amyloid-beta and tau in tanycytes and neuronal terminals. Disrupted tanycyte function may contribute to hypothalamic dysfunction and neuroendocrine disturbances observed in AD patients[@gahete2023]. Altered thyroid hormone transport across the ME may affect cerebral metabolism and contribute to cognitive decline[@martha2022].
Parkinson's Disease
The ME is affected in PD through alpha-synuclein accumulation in hypothalamic neurons that project to this region. Neuroendocrine abnormalities in PD, including altered cortisol rhythms and growth hormone secretion, may reflect ME dysfunction. The ME's role in dopamine transport to the pituitary may be relevant to PD-related endocrine changes[@jellinger2021].
Huntington's Disease
Huntington's disease involves early hypothalamic pathology that affects the ME. Altered hormone levels in HD patients, including cortisol and testosterone, may relate to ME dysfunction. Tanycyte abnormalities have been reported in HD mouse models[@van2022].
Multiple System Atrophy
MSA features prominent autonomic dysfunction related to hypothalamic involvement. The ME, as a key autonomicregulatory site, shows pathology in MSA. Dysregulated hormone release through the ME may contribute to orthostatic hypotension and other autonomic symptoms[@benarroch2023].
Hypothalamic-Pituitary-Adrenal Axis
The ME is critical for HPA axis regulation, as CRH and vasopressin neurons project to the portal capillaries. Chronic stress and neurodegeneration can dysregulate this system, leading to elevated cortisol and hippocampal atrophy. The ME serves as a convergence point for stress-related neurodegeneration[@de2021].
Molecular Characteristics
Key molecular markers of ME cells include:
- vimentin and GFAP: tanycyte markers
- TRH: hypothalamic-releasing hormone neurons
- DIO2: type 2 deiodinase, converts T4 to T3 in tanycytes
- LEP-R: leptin receptor in tanycytes
- GLUT1/SLC2A1: glucose transporter[@poleni2022]
Therapeutic Implications
The ME represents a potential target for neurodegenerative disease therapy. Hormone replacement through the portal system could modulate neuroendocrine function. Tanycyte-targeted drug delivery could bypass the blood-brain barrier. Gene therapy approaches to restore ME function are under investigation[@banks2023].
See Also
- [Alzheimer's Disease](/diseases/alzheimers-disease)
- [Parkinson's Disease](/diseases/parkinsons-disease)
External Links
- [PubMed](https://pubmed.ncbi.nlm.nih.gov/)
- [KEGG Pathways](https://www.genome.jp/kegg/pathway.html)